Blockage of epinephrine-induced hyperglycemia during exposure to simulated altitudes

Abstract

Hyperglycemia elicited by subcutaneous injection of epinephrine (10 µg/rat) was completely abolished during the exposure of the rat to a simulated high altitude (220–250 mm Hg). Addition of 5–7% CO₂ to the inspired gas during the altitude stress restored the hyperglycemic activity of epinephrine, suggesting that the alkalosis or hypocapnia provoked by hyperventilation, but not hypoxia itself, would be involved in the prevention of the hyperglycemic action of epinephrine. Glucose tolerance tests and in vitro experiments using isolated rat diaphragm showed that the inhibitory action of epinephrine on peripheral glucose utilization was abolished by shifting the pH of body fluids or incubation media toward higher levels. It was concluded that alkalosis, either directly or indirectly, abolished the hyperglycemic action of epinephrine as a consequence of the release of the inhibitory action of epinephrine on muscle glucose utilization.